Given these pieces of information, together with the protective effect of OAT10 c.1129C>T on gout susceptibility (Higashino et al., 2020), our data support the physiological importance of OAT10 as a urate transporter in the kidney, although the β of OAT10 was not so large compared with cases of causal genes for renal hypouricemia (which means that OAT10 has a smaller contribution to renal urate re-uptake than URAT1 and GLUT9). Here, SLC22A13 is linked to gout.